Blood Component Therapy
Transfusion Related Risks
Blood Centers began clinical trials in April 1999 to screen blood with a PCR test for HCV RNA and HIV DNA. Although confirmed data are not available, the current estimated risks/unit are:
- HIV, <1:1,900,000
- Hepatitis C, <1:1,000,000
The most recent estimated risks/unit for other viral transmissions are:
- Hepatitis B, 1:1,000,000
- HTLV I & II, 1:641,000
West Nile Virus (WNV) can be transmitted by blood transfusions but the risk is extremely low. PCR testing is performed to detect WNV. At the current time no cases of WNV in humans has been reported in Washington State. Rarely, Chagas disease (Trypanosoma cruzi) has been transmitted through transfusion. Testing is done on donors who have lived in or were born in endemic areas (Central & South America).
In CMV sero-negative, immunosuppressed transplant and HIV positive patients, the risk of CMV infection is high. In the King County area the CMV sero-positive incidence in the donor population is about 50%. Leukocyte depletion of blood is equivalent to CMV sero-negative blood in preventing CMV infection through transfusion, but is more expensive and indicated only if CMV sero-negative blood or platelets are not available. In some organ transplant recipients CMV sero-negative blood is transfused to prevent infection with secondary strains.
Bacterial contamination was previously estimated to occur in <1:2000 platelet concentrates and ≤ 1:38,565 rbc units. Bacterial testing ofplatelet concentrates has significantly decreased this risk from platelet transfusions.
A transfusion should be stopped immediately whenever a transfusion reaction is suspected.
A hemolytic transfusion reactionoccurs following transfusion of an incompatible blood component. Most are due to naturally occurring antibodies in the ABO antigen system. An acute hemolytic transfusion reaction may cause hemoglobin induced renal failure and a consumptive coagulopathy (DIC). Signs and symptoms include fever, hypotension, nausea, vomiting, tachycardia, dyspnea, chest or back pain, flushing and severe anxiety. Hemoglobinuria may be noted and, in the anesthetized patient, may be the first sign of hemolysis. The diagnosis can be quickly made by centrifuging a tube of blood and examining the plasma for a reddish discoloration. A fresh sample of blood should be sent to the Blood Center for testing and all paper work and the patient’s identification checked. Treatment involves fluids, diuresis and transfusion support for bleeding. A fatal hemolytic transfusion reaction occurs about once in 600,000 transfusions. Most errors are clerical or due to misidentification of a patient at the bedside.
Delayed hemolytic transfusion reactionsusually occur in patients who have been previously sensitized to an antigen through transfusion or pregnancy. They can result in symptomatic or asymptomatic hemolysis several days after a subsequent transfusion due to an anamnestic recall of the antibody.
Transfusion of Rh positive red blood cells to an Rh negative woman of childbearing age can result in sensitization and hemolytic
disease of the newborn in future pregnancies.
Febrile transfusion reactionsusually occur due to sensitization to antigens on cell components, particularly leukocytes. Leukocyte depletion of red blood cells by filtration may be helpful in patients for whom this is a problem. Leukocyte reduced single donor pheresed platelets are a possible alternative to leukocyte depletion by filtration of pooled random donor platelets and are comparable in cost. Occasionally, removal of most of the plasma (volume reduction) may be necessary to remove cytokines in platelet preparations for patient with persistent febrile reactions.
Rarely, a febrile episode during a transfusion, particularly with platelets, is due to bacterial contamination. Generally these reactions are quite severe with high fever, rigors and/or other systemic symptoms such as hypotension, nausea or vomiting. If a bacterially contaminated component is suspected, the transfusion should be stopped and the bag sent for gram stain and culture. The Blood Center should be notified. The patient should have blood cultures obtained and, if appropriate, IV antibiotic therapy begun.
Transfusion Related Acute Lung Injury (TRALI)occurs when donor plasma contains an antibody, usually against the patient’s HLA or leukocyte specific antigens. Less often, the patient may have antibodies against donor leukocytes in the component. Symptoms of dyspnea, hypotension and fever typically begin 30 minutes to 6 hours after transfusion and the chest x-ray shows diffuse non-specific infiltrates. Ventillatory support may be required for several days before resolution. Therapy is primarily supportive. The Blood Center should be notified so that the donor may be tested for antibodies against the patient.
Urticarial and allergic type reactions are the most common, usually due to allergies to specific proteins in the donor’s plasma and can be avoided with future transfusions by pretreatment with antihistamines or steroids. Only if severe (anaphylaxis), are washed RBC’s and platelets to remove all plasma indicated. IgA deficiency should be considered in the case of anaphylactic reactions.
Transfusions have been known to induce immune tolerance following the observation made more than 20 years ago that multiply transfused kidney transplant recipients had an increased graft survival rate. In addition, some studies suggest that transfusion may increase the rate of post-operative bacterial infection. There is also evidence from animal studies that transfusion increases the risk of metastatic disease, although data in humans are inconclusive.
Sensitization to foreign donor HLA antigens, or alloimmunization, can lead to poor platelet transfusion increments. Patients may respond to pheresed platelets from HLA-matched donors or family members. HLA alloimmunization also decreases the likelihood of finding a compatible donor for heart or renal transplant.
Removal of donor leukocytes has been shown to decrease the immunomodulatory effects of blood transfusions but the clinical usefulness is clear only in the prevention of alloimmunization in patients undergoing chemotheraphy for AML.